Gynaecology Flashcards
Common presenting complaints in gynecology?
▪ Heavy/painful/irregular or absent periods
▪ Pelvic pain/pain on intercourse
▪ Urinary incontinence
▪ ‘something coming down’ (prolapse)
▪ Infertility
▪ Request for sterilisation
▪ Bleeding or pain in early pregnancy
▪ Postmenopausal bleeding
▪ Vaginal discharge
What should be asked about in a menstrual history?
First and last day of last menstrual period (LMP)
Any abnormal bleeding: intermenstrual or post coital bleeding
Menarche (age at first period)
Frequency – average 28 days <24 days Frequent, >38 days Infrequent
Duration of bleeding – average 5 days (>8 days Prolonged, <4.5 days shortened)
Volume – average 40ml menstrual blood loss over course of menses
>80ml heavy (Hb and Ferritin affected), <5ml Light
Women may describe ‘flooding’ and clots passed
What might you ask a patient about contraception when history taking?
Current method and duration of use
Previous methods - what method, length of use, why it was stopped, when it was stopped
Any problems with contraception
Hx of migraines with aura if considering COCP
What might you ask a patient about cervical smears when taking a gynae history?
When a smear was last taken
What was the result
What might be relevant to obstetric history?
Gravidity (number of pregnancies)
Parity (number of births of gestation last 24 weeks)
Pregnancy outcomes
Birth weights
Modes of delivery - vaginal, assisted vaginal (forceps), c section
When births occurred (at term)
Prv baby weight
Any miscarriages - when - medical, spontaneous, surgical (D&C)
Antenatal checks - chromosomal abnormalities testing?? Bloods, 11-14 week dating scan, 20 week abnormality scan
What might be relevant in a past gynaecology history?
Past gynaecological problems, their investigations and treatment
Previous gynaecological operations
Past genitourinary infections
Smears
Contraception
Menstural history
Sexual history including STIs
Basic structure of gynaecological history?
Demographic and reproductive identifiers
Presenting complaint (elaborate, impact on QOL and normal functioning)
Menstrual history
Contraception
Sexual history
Possibility of pregnancy
Cervical smear
Obstetric history and plans for future pregnancies
Previous gynaecological history
Past medical history
DHx inc allergies
Social hx including smoking and alcohol
FHx
System inquires
ICE
Describe the mechanism of action in tranexamic acid in the management of heavy menstrual blood loss
Fibrinolytic drug
TXA is a synthetic reversible competitive inhibitor to the lysine receptor found on plasminogen. The binding of this receptor prevents plasmin (activated form of plasminogen) from binding to and ultimately stabilizing the fibrin matrix and therefore bleeding.
Describe the mechanism of action in mefanamic acid in the management of heavy menstrual blood loss and dysmenorrhea?
NSAID, works by inhibition of prostaglandin synthesis + reduces the activity of prostaglandins in the uterus lining which are elevated in women with heavy bleeding.
Prostaglandins are hormones which cause pain and inflammation
What is hematometra and why might it occur?
Hematometra is a collection or retention of blood in the uterus most commonly due to an imperforate hymen or transverse vaginal septum.
Acquired causes leading to cervical stenosis include radiation treatment, ablation, cervical conization, or malignancies
Causes of menorrhagia?
Dysfunctional uterine bleeding (no identifiable cause)
Extremes of reproductive age
Fibroids
Endometriosis and adenomyosis
Pelvic inflammatory disease (infection)
Contraceptives, particularly the copper coil
Anticoagulant medications
Bleeding disorders (e.g. Von Willebrand disease)
Endocrine disorders (diabetes and hypothyroidism)
Connective tissue disorders
Endometrial hyperplasia or cancer
Polycystic ovarian syndrome
The PALM-COEIN system divides the causes into structural (‘PALM’) and non-structural (‘COEIN’) - what are the structural causes of menorrhagia?
Polyps
Adenomyosis
Leiomyoma (fibroid)
Malignancy of endometrial hypoplasia (this includes bleeding from vaginal or cervical malignancies, or that provoked by ovarian tumours)
The PALM-COEIN system divides the causes into structural (‘PALM’) and non-structural (‘COEIN’) - what are the non-structural causes of menorrhagia?
Coagulopathy (Von Willebrand’s disease is the most common coagulopathy to cause heavy menstrual bleeding, also consider warfarin therapy)
Ovarian dysfunction (PCOS, hypothyroidism)
Endometriosis
Iatrogenic (E.g. contraceptive hormones, copper IUD.)
No identifiable cause (DUB)
What features might suggest an underlying coagulopathy in a patient presenting with HMB (menorrhagia)
HMB since menarche
History of post-partum haemorrhage
Surgical related bleeding or dental related bleeding; Easy bruising/epistaxis
Bleeding gums
Family history of bleeding disorder
How might fibroids present?
Bulky uterus O/E
HMB
Hx of pressure symptoms (urinary freq, constipation)
What volume of blood loss during a period would affects Hb and Ferritin?
> 80ml
Anaemia from 120ml
Most patients presenting with menorrhagia (heavy menstrual bleeding) should be examined (pelvic examination with speculum and bimanual) - what should be looked out for?
Pallor (anaemia)
Palpable uterus or pelvic mass
Try to ascertain if the uterus is smooth or irregular (fibroids)
A tender uterus or cervical excitation point toward adenomyosis/endometriosis
Inflamed cervix/cervical polyp/cervical tumour
Vaginal tumour
Ascities
Main features of HMB (menorrhagia)
Bleeding during menstruation deemed to be excessive for the individual woman (>80ml): changing pads every 1-2 hours, bleeding lasting more than 7 days or passing very large clots.
Fatigue.
Shortness of breath (if associated anaemia).
Main risk factors for heavy menstrual bleeding (menorrhagia)?
The two main risk factors for heavy menstrual bleeding are age (more likely at menarche and approaching the menopause), and obesity.
There are also other risk factors that relate to the specific causes of HMB. One example would be previous caesarean section – as a risk factor for adenomyosis.
What is HMB?
Heavy menstrual bleeding - excessive menstrual loss, bleeding not related to pregnancy and occurring only within the woman’s reproductive years (ie. not post-menopausal bleeding).
Diagnosis based on symptoms - such as changing pads every 1-2 hours, bleeding lasting more than 7 days, passing large blood clots.
Most patients presenting with menorrhagia (heavy menstrual bleeding) should be examined (pelvic examination with speculum and bimanual) - when might they not require PV examination?
Straightforward hx HMB without other risk factors or symptoms
Patients who are young and not sexually active
What investigation should be performed in all women with HMB and why?
Full blood count - to look for iron deficiency anaemia
What bloods might be performed in a women presenting with HMB?
Full blood count:
Anaemia tends to present after menstrual blood loss of 120ml.
Thyroid function test:
If other signs and symptoms of underactive thyroid.
Other hormone testing:
Not routine but considered if other clinical features e.g. suspicion of Polycystic ovary syndrome.
Coagulation screen + test for Von Willebrand’s:
If suspicion of clotting disorder on history taking.
HMB: imaging, histology and microbiology
Ultrasound pelvis
Transvaginal US is most clinically useful for assessing the endometrium and ovaries.
It should be considered if the uterus or a pelvic mass is palpable on examination, or if pharmacological treatment has failed.
Cervical smear
No need to repeat if up to date.
High vaginal and endocervical swabs for infection.
Pipelle endometrial biopsy:
(if persistent intermenstrual bleeding, >45 years old, and/or failure of pharmacological treatment.)
Hysteroscopy and endometrial biopsy:
(Typically performed when ultrasound identifies pathology, or is inconclusive)
Indications for pipelle endometrial biopsy in a patient presenting with HMB?
Persistent IMB, >45 years old, and/or failure of pharmacological treament
When should outpatient hysteroscopy be arranged in a patient presenting with HMB?
Suspected submucosal fibroids
Suspected endometrial pathology, such as endometrial hyperplasia or cancer
Persistent intermenstrual bleeding
When should pelvic and transvaginal ultrasound be arranged in a patient presenting with HMB?
Possible large fibroids (palpable pelvic mass)
Possible adenomyosis (associated pelvic pain or tenderness on examination)
Examination is difficult to interpret (e.g. obesity)
Hysteroscopy is declined
Medical management of HMB?
Management of identifiable cause
Symptomatic relief (non contraceptive): tranexamic acid or mefenamic acid
Contraception: Minera coil (1st line), COCP, cyclical oral progestogens, progesterone only contraception (depo, implant POP)
NB: oral norethisterone (Taken day 5-26 of cycle) does not work as a contraceptive when taken in this manner
Management of HMB where medical management has failed?
Endometrial ablation
Hysterectomy (subtotal or total, ovaries not removed unless abnormal. Can be performed through abdominal incision or through the vagina
Fibroids: myomectomy and uterine artery embolism
When is referral to secondary care for further investigation and management indicated for patients with HMB?
Referral to secondary care for further investigation and management is indicated if treatment is unsuccessful, symptoms are severe or there are large fibroids (more than 3 cm).
Levonorgestral-releasing intrauterine system (LNG-IUS) - use in HMB
First line contraceptive option
Also acts as a contraceptive.
Is licensed for 5 years treatment.
Thins endometrium and can shrink fibroids.
When is oral norethisterone taken when used to manage HMB
(Taken day 5-26 of cycle)
Tranexamic acid, mefanamic acid - advantages in treating HMB?
No effect on fertility
Non-hormonal
Mefenamic acid also analgesic
What is a hysterectomy?
A hysterectomy is the surgical removal of the uterus. It is a very common procedure, performed for a variety of indications.
It can be classified by the amount of tissue resected
Total hysterectomy
Sub-total hysterectomy
Total hysterectomy and bilateral salpingo-oophorectomy
Radical hysterectomy
There are three main approaches to a hysterectomy. The principles and steps for each approach are the same (but in a different order).
Abdominal – via an incision in the abdomen.
Vaginal – via incision through the superior part of the vagina.
Laparoscopic – via small incisions in the abdomen, and using laparoscopes and a uterine manipulator.
What is a total hysterectomy?
removal of the uterus and cervix
What is a sub-total hysterectomy
removal of the body of the uterus only (leaving the cervix behind)
What is a total hysterectomy and bilateral salpingo-oophorectomy?
removal of the uterus, cervix, fallopian tubes and ovaries.
What is a radical hysterectomy and why might it be performed?
Removal of:
Uterus
Cervix
Parametrium
Vaginal cuff
Part of or entire fallopian tubes
Ovaries may be removed or left behind (depending on the patients age)
Mobilization + discharge - hysterectomy?
Mobilisation should be encouraged as soon as possible.
Discharge is usually after 1-2 days for vaginal and laparoscopic hysterectomy, and 2-5 days for abdominal hysterectomy (depending on the type of incision – generally longer stay if midline incision).
What incision is used to perform and abdominal hysterectomy?
Depends on uterus size and indication
Low transverse incision
Midline incision (may be necessitated in a large fibroid uterus for example)
What type of anesthetic is used in a hysterectomy?
Abdominal and laproscopic hysterectomy are perfomed under general anestethic
Vaginal hysterectomy may be performed under regional anaesthesia (spinal/ epidural). A general anaesthetic is not required.
Indications for hysterectomy?
Heavy menstrual bleeding
Pelvic pain
Uterine prolapse (vaginal hysterectomy
)
Gynaecological malignancy (usually ovarian, uterine or cervical)
Risk reducing surgery, usually in cases of BRCA 1 or 2 mutations, or Lynch syndrome.
Hysterectomy may also be performed as a life saving procedure in the management of major postpartum haemorrhage.
There are some potential complications of a hysterectomy. As for any surgical procedure, the general complications include risk of haemorrhage, infection and pain. There is also a general anaesthetic risk. What do the procedure specific complications include?
Damage to bladder and/or uterter and/or long term distrbance to bladder function
Damage to the bowel
Hemorrhage requiring blood tranfusion (relatively common)
Return to theatre: bleeding/wound dehissince
Pelvic abscess/infection
VTE or PE
Risk of death within 6 weeks, 32 women in every 100 000 (rare). The main causes of death are pulmonary embolism and cardiac disease.
If the ovaries are conserved, menopause may occur earlier (by 1-2 years) due to a change in the blood supply to the ovaries.
What is dysmenorrhea?
Dysmenorrhoea or “painful periods” is the most common of all gynaecological symptoms. It is generally described as a crampy lower abdominal pain, which starts at the onset of menstruation.
It can be classified as either:
Primary – menstrual pain occurring with no underlying pelvic pathology.
Secondary – menstrual pain that occurs with an associated pelvic pathology.
Aetiology and pathophysiology of dysmenorrhea
In the absence of fertilisation of the egg, the corpus luteum regresses, and there is a subsequent decline in oestrogen and progesterone production.
The endometrial cells are sensitive to this decline in progesterone, and respond with prostaglandin release. Prostaglandins have two main actions in the uterus:
Spiral artery vasospasm – leading to ischaemic necrosis and shedding of the superficial layer of the endometrium.
Increased myometrial contractions.
Primary dysmenorrhoea is thought to occur secondary to the excessive release of prostaglandins (PGF2α and PGE2) by endometrial cells.
What are the risk factors for primary dysmenorrhoea?
Early menarche
Long menstrual phase
Heavy periods
Smoking
Nuliparity
Clinical features of dysmenorrhoea?
The typical description of dysmenorrhoea is lower abdominal or pelvic pain, which can radiate to lower back or anterior thigh.
Pain is crampy in nature. It usually lasts for 48-72 hours around the menstrual period, and is characteristically worst at the onset of menses.
The pain can be associated with other symptoms, such as; malaise, nausea, vomiting, diarrhoea, dizziness.
Abdominal and pelvic examinations (including speculum examination of cervix) are performed but are usually unremarkable. Uterine tenderness may be present.
Note: Dysmenorrhoea may resolve following pregnancy.
Causes of secondary dysmenorrhoea?
Endometriosis
Adenomyosis
Pelvic inflammatory disease
Adhesions
Dysmenorrhoea - investigations?
No investigations are specific to primary dysmenorrhoea and therefore the work up is focused on ruling out underlying pathology.
If the patient is at high risk of a sexually transmitted infection, then a high vaginal swab and endocervical swabs are indicated to screen for underlying infection.
If on examination a pelvic mass is palpated, a transvaginal ultrasound scan (TVS) should be performed to investigate further.
Management of dysmenorrhoea?
Lifestyle Changes:
Stop smoking (there is a clear relationship between smoking and dysmenorrhoea).
Pharmacological:
Anagelsia (First line):
NSAIDs (ibuprofen, naproxen, mefenamic acid). They work by inhibiting the production of prostaglandins; which have been implicated in the pathogenesis of primary dysmenorrhoea.
And/or paracetamol
3-6 month trial of hormonal contraception (Second line):
Monophasic combined oral contraceptive pill is most commonly used first line.
Intrauterine system (e.g Mirena coil) may also be effective.
Non-Pharmacological
Local application of heat (water bottles or heat patch)
Transcutaneous Electrical Nerve Stimulation (TENS)
What is amenorrhoea?
Amenorrhoea refers to a lack of menstrual periods.
Primary amenorrhoea is when the patient has never developed periods.
Secondary amenorrhoea is when the patient previously had periods that subsequently stopped.
What is abnormal uterine bleeding and why might it occur?
Abnormal uterine bleeding refers to irregularities in the menstrual cycle, affecting frequency, duration, regularity of the cycle length and the volume of menses. Irregular menstrual periods indicate anovulation (a lack of ovulation) or irregular ovulation. This occurs due to disruption of the normal hormonal levels in the menstrual cycle, or ovarian pathology. It can be due to:
Extremes of reproductive age (early periods or perimenopause)
Polycystic ovarian syndrome
Physiological stress (excessive exercise, low body weight, chronic disease and psychosocial factors)
Medications, particularly progesterone only contraception, antidepressants and antipsychotics
Hormonal imbalances, such as thyroid abnormalities, Cushing’s syndrome and high prolactin
What is IMB?
Intermenstrual bleeding (IMB) refers to any bleeding that occurs between menstrual periods. This is a red flag that should make you consider cervical and other cancers, although other causes are more common.
What are the key causes of IMB?
Hormonal contraception
Cervical ectropion, polyps or cancer
Sexually transmitted infection
Endometrial polyps or cancer
Vaginal pathology, including cancers
Pregnancy
Ovulation can cause spotting in some women
Medications, such as SSRIs and anticoagulants
What is dysmenorrhea and why might it occur?
Dysmenorrhoea describes painful periods. The causes are:
Primary dysmenorrhoea (no underlying pathology)
Endometriosis or adenomyosis
Fibroids
Pelvic inflammatory disease
Copper coil
Cervical or ovarian cancer
What is menorrhagia and why might it occur?
Menorrhagia refers to heavy menstrual bleeding. This can be caused by:
Dysfunctional uterine bleeding (no identifiable cause)
Extremes of reproductive age
Fibroids
Endometriosis and adenomyosis
Pelvic inflammatory disease (infection)
Contraceptives, particularly the copper coil
Anticoagulant medications
Bleeding disorders (e.g. Von Willebrand disease)
Endocrine disorders (diabetes and hypothyroidism)
Connective tissue disorders
Endometrial hyperplasia or cance
Polycystic ovarian syndrome
What is post coital bleeding and why might it occur?
Postcoital bleeding (PCB) refers to bleeding after sexual intercourse. This is a red flag that should make you consider cervical and other cancers, although other causes are more common. Often no cause is found. The key causes are:
Cervical cancer, ectropion or infection
Trauma
Atrophic vaginitis
Polyps
Endometrial cancer
Vaginal cancer
What might cause pelvic pain?
Urinary tract infection
Dysmenorrhoea (painful periods)
Irritable bowel syndrome (IBS)
Ovarian cysts
Endometriosis
Pelvic inflammatory disease (infection)
Ectopic pregnancy
Appendicitis
Mittelschmerz (cyclical pain during ovulation)
Pelvic adhesions
Ovarian torsion
Inflammatory bowel disease (IBD)
Excessive, discoloured or foul-smelling discharge may indicate what?
Bacterial vaginosis
Candidiasis (thrush)
Chlamydia
Gonorrhoea
Trichomonas vaginalis
Foreign body
Cervical ectropion
Polyps
Malignancy
Pregnancy
Ovulation (cyclical)
Hormonal contraception
What is pruritus vulvae and why might it occur?
Pruritus vulvae refers to itching of the vulva and vagina
Irritants such as soaps, detergents and barrier contraception
Atrophic vaginitis
Infections such as candidiasis (thrush) and pubic lice
Skin conditions such as eczema
Vulval malignancy
Pregnancy-related vaginal discharge
Urinary or faecal incontinence
Stress
How is primary amenorrhoea definied?
Primary amenorrhoea is defined as not starting menstruation:
By 13 years when there is no other evidence of pubertal development
By 15 years of age where there are other signs of puberty, such as breast bud development
What is hypogonadism and what are the two reasons it might occur?
Hypogonadism refers to a lack of the sex hormones, oestrogen and testosterone, that normally rise before and during puberty. A lack of these hormones causes a delay in puberty. The lack of sex hormones is fundamentally due to one of two reasons:
Hypogonadotropic hypogonadism: a deficiency of LH and FSH
Hypergonadotropic hypogonadism: a lack of response to LH and FSH by the gonads (the testes and ovaries)
What is hypogonadotrophic hypogonadism?
Hypogonadotropic hypogonadism involves deficiency of LH and FSH, leading to deficiency of the sex hormones (oestrogen). LH and FSH are gonadotrophins produced by the anterior pituitary gland in response to gonadotropin releasing hormone (GnRH) from the hypothalamus. Since no gonadotrophins are simulating the ovaries, they do not respond by producing sex hormones (oestrogen). Therefore, “hypogonadotropism” causes “hypogonadism”.
A deficiency of LH and FSH is the result of abnormal functioning of the hypothalamus or pituitary gland. This could be due to:
Hypopituitarism (under production of pituitary hormones)
Damage to the hypothalamus or pituitary, for example, by radiotherapy or surgery for cancer
Significant chronic conditions can temporarily delay puberty (e.g. cystic fibrosis or inflammatory bowel disease)
Excessive exercise or dieting can delay the onset of menstruation in girls
Constitutional delay in growth and development is a temporary delay in growth and puberty without underlying physical pathology
Endocrine disorders such as growth hormone deficiency, hypothyroidism, Cushing’s or hyperprolactinaemia
Kallman syndrome
What is hypergonadotropic hypogonadism and why might occur?
Hypergonadotropic hypogonadism is where the gonads fail to respond to stimulation from the gonadotrophins (LH and FSH). Without negative feedback from the sex hormones (oestrogen), the anterior pituitary produces increasing amounts of LH and FSH. Consequently, you get high gonadotrophins (“hypergonadotropic”) and low sex hormones (“hypogonadism”).
Hypergonadotropic hypogonadism is the result of abnormal functioning of the gonads. This could be due to:
Previous damage to the gonads (e.g. torsion, cancer or infections such as mumps)
Congenital absence of the ovaries
Turner’s syndrome (XO)
What is Kallman syndrome?
Kallman syndrome is a genetic condition causing hypogonadotrophic hypogonadism, with failure to start puberty.
It is associated with a reduced or absent sense of smell (anosmia).
What is congenital adrenal hyperplasia and why might it occur?
Congenital adrenal hyperplasia is caused by a congenital deficiency of the 21-hydroxylase enzyme.
This causes underproduction of cortisol and aldosterone, and overproduction of androgens from birth. It is a genetic condition inherited in an autosomal recessive pattern. In a small number of cases, it involves a deficiency of 11-beta-hydroxylase rather than 21-hydroxylase.
In severe cases, the neonate is unwell shortly after birth, with electrolyte disturbances and hypoglycaemia. In mild cases, female patients can present later in childhood or at puberty with typical features:
Tall for their age
Facial hair
Absent periods (primary amenorrhoea)
Deep voice
Early puberty
What is androgen insensitivity syndrome?
Androgen insensitivity syndrome is a condition where the tissues are unable to respond to androgen hormones (e.g. testosterone), so typical male sexual characteristics do not develop. It results in a female phenotype, other than the internal pelvic organs.
Patients have normal female external genitalia and breast tissue. Internally there are testes in the abdomen or inguinal canal, and an absent uterus, upper vagina, fallopian tubes and ovaries.
Structural pathology resulting in primary amenorrhoea?
Structural pathology in the pelvic organs can prevent menstruation. If the ovaries are unaffected, there will be typical secondary sexual characteristics, but no menstrual periods. There may be cyclical abdominal pain as menses build up but are unable to escape through the vagina. Structural pathology that can cause primary amenorrhoea include:
Imperforate hymen
Transverse vaginal septae
Vaginal agenesis
Absent uterus
Female genital mutilation
When would primary amenorrhea be investigated?
The threshold for initiating investigations is no evidence of pubertal changes in a girl aged 13.
Investigation can also be considered when there is some evidence of puberty but no progression after two years.
How might primary amenorrhea be investigated?
BLOODS FOR UNDERLYING MEDICAL CONDITIONS
Full blood count and ferritin for anaemia
U&E for chronic kidney disease
Anti-TTG or anti-EMA antibodies for coeliac disease
BLOODS FOR HORMONAL ABNORMALITIES
FSH and LH (will be low in hypogonadotropic hypogonadism and high in hypergonadotropic hypogonadism)
Thyroid function tests
Insulin-like growth factor I is used as a screening test for GH deficiency
Prolactin (raised in hyperprolactinaemia)
Testosterone is raised in polycystic ovarian syndrome, androgen insensitivity syndrome and congenital adrenal hyperplasia
Genetic testing with a microarray test to assess for underlying genetic conditions:
Turner’s syndrome (XO)
IMAGING
Xray of the wrist to assess bone age and inform a diagnosis of constitutional delay
Pelvic ultrasound to assess the ovaries and other pelvic organs
MRI of the brain to look for pituitary pathology and assess the olfactory bulbs in possible Kallman syndrome
Primary Amenorrhoea - management
Management of primary amenorrhoea involves establishing and treating the underlying cause.
Where necessary, replacement hormones can induce menstruation and improve symptoms.
Patients with constitutional delay in growth and development may only require reassurance and observation.
Where the cause is due to stress or low body weight secondary to diet and exercise, treatment involves a reduction in stress, cognitive behavioural therapy and healthy weight gain.
Where the cause is due to an underlying chronic or endocrine condition, management involves optimising treatment for that condition.
In patients with hypogonadotrophic hypogonadism, such as hypopituitarism or Kallman syndrome, treatment with pulsatile GnRH can be used to induce ovulation and menstruation. This has the potential to induce fertility.
Alternatively, where pregnancy is not wanted, replacement sex hormones in the form of the combined contraceptive pill may be used to induce regular menstruation and prevent the symptoms of oestrogen deficiency.
In patients with an ovarian cause of amenorrhoea, such as polycystic ovarian syndrome, damage to the ovaries or absence of the ovaries, the combined contraceptive pill may be used to induce regular menstruation and prevent the symptoms of oestrogen deficiency.
What might cause primary amenorrhoea?
Constitutional delay in puberty
Chromosomal or genetic abnormalities such as Turner syndrome (45 XO) (gonadal dysgenisis) Kallmann syndrome and androgen insensitivity syndrome.
Disruption of the functioning of the hypothalamic or pituitary glands (functional hypothalamic amenorrhoea) For example as a result of:
- Anorexia and other eating disorders,
- Excessive exercise
- Extreme physical or psychological stress
Structural abnormalities of the genital tract such as:
- Imperforate hymen obstructing menstrual flow (leading to haematocolpos)
- Uterine agenesis
- Pregnancy
What is secondary amenorrhea? When should it be investigated?
Secondary amenorrhea is defined as no menstruation for more than three months after previous regular menstrual periods.
Consider assessment and investigation after three to six months.
In women with previously infrequent irregular periods, consider investigating after six to twelve months.
Causes of secondary amenorrhea?
Pregnancy is the most common cause
Menopause and premature ovarian failure
Hormonal contraception (e.g. IUS or POP)
Hypothalamic or pituitary pathology (hypothalamic amenorrhoea - (e.g. secondary stress, excessive exercise)),
Ovarian causes such as polycystic ovarian syndrome (androgen levels raised)
Uterine pathology such as Asherman’s syndrome (intrauterine adhesions)
Thyroid pathology (thyrotoxicosis, hypothyroidism)
Hyperprolactinaemia
Sheenans syndrome
Hypothalamic aetiology of secondary amenorrhoea?
The hypothalamus reduces the production of GnRH in response to significant physiological or psychological stress.
This leads to hypogonadotropic hypogonadism and amenorrhoea. The hypothalamus responds this way to prevent pregnancy in situations where the body may not be fit for it, for example:
Excessive exercise (e.g. athletes)
Low body weight and eating disorders
Chronic disease
Psychological stress
Pituitary causes of secondary amenorrhoea?
Pituitary causes of secondary amenorrhoea include:
Pituitary tumours, such as a prolactin-secreting prolactinoma
Pituitary failure due to trauma, radiotherapy, surgery or Sheehan syndrome
How can hyperprolactinemia cause secondary amenorrhea?
Why might it occur?
How is it managed?
High prolactin levels act on the hypothalamus to prevent the release of GnRH. Without GnRH, there is no release of LH and FSH.
This causes hypogonadotropic hypogonadism. Only 30% of women with a high prolactin level will have galactorrhea (breast milk production and secretion).
The most common cause of hyperprolactinaemia is a pituitary adenoma secreting prolactin. Where there are high prolactin levels, a CT or MRI scan of the brain is used to assess for a pituitary tumour.
Often there is a microadenoma that will not appear on the initial scan, and follow up scans are required to identify tumours that may develop later.
Often no treatment is required for hyperprolactinaemia.
Dopamine agonists such as bromocriptine or cabergoline can be used to reduce prolactin production
These medications treat hyperprolactinaemia, Parkinson’s disease and acromegaly.
How is secondary amenorrhoea investigated?
Detailed history and examination to assess for potential causes
Ultrasound of the pelvis to diagnose polycystic ovarian syndrome
Hormonal blood tests:
- Beta human chorionic gonadotropin (HCG) urine or blood tests (pregnancy)
-LH and FSH
- Prolactin (can be measured to assess for hyperprolactinaemia, followed by an MRI to identify a pituitary tumour)
- Thyroid stimulating hormone (TSH) (screen for thyroid pathology) This is followed by T3 and T4 when the TSH is abnormal)
- Testosterone: (Raise testosterone indicates polycystic ovarian syndrome, androgen insensitivity syndrome or congenital adrenal hyperplasia)
Interpreting abnormal FSH and LH in the context of secondary amenorrhea?
High FSH suggests primary ovarian failure
High LH, or LH:FSH ratio, suggests polycystic ovarian syndrome
What should you advise women taking hormonal replacement to manage PCOS to minimize risk and why?
Require a withdrawal bleed every 3 – 4 months to reduce the risk of endometrial hyperplasia and endometrial cancer.
Medroxyprogesterone for 14 days, or regular use of the combined oral contraceptive pill, can be used to stimulate a withdrawal bleed.
Management of secondary amenorrhea?
Management of secondary amenorrhoea involves establishing and treating the underlying cause. Where necessary, replacement hormones can induce menstruation and improve symptoms.
What non-gynecological condition can secondary amenorrhea increase the risk of, and when is treatment indicated to minimize this risk? What treatment is used?
Patients with amenorrhoea associated with low oestrogen levels are at risk increased risk of osteoporosis.
Where the amenorrhoea lasts more than 12 months, treatment is indicated to reduce the risk of osteoporosis:
Ensure adequate vitamin D and calcium intake
Hormone replacement therapy or the combined oral contraceptive pill
What is premenstural syndrome and why does it occur?
Premenstrual syndrome (PMS) describes the psychological, emotional and physical symptoms that occur during the luteal phase of the menstrual cycle, particularly in the days prior to the onset of menstruation. These symptoms can be distressing and significantly impact quality of life.
Most women will experience some of the symptoms of premenstrual syndrome. The critical aspects are the severity of the symptoms, and the impact these symptoms have on the woman’s functioning and quality of life.
The symptoms of PMS resolve once menstruation begins. Symptoms are not present before menarche, during pregnancy or after menopause. These are key things to note when you take a history.
Premenstrual syndrome is though to the caused by fluctuation in oestrogen and progesterone hormones during the menstrual cycle. The exact mechanism is not known, but it may be due to increased sensitivity to progesterone or an interaction between the sex hormones and the neurotransmitters serotonin and GABA.
How might PMS present?
There is a long list of symptoms that can occur with premenstrual syndrome, and these will vary with the individual. Common symptoms include:
Low mood
Anxiety
Mood swings
Irritability
Bloating
Fatigue
Headaches
Breast pain
Reduced confidence
Cognitive impairment
Clumsiness
Reduced libido
These symptoms can occur in the absence of menstruation after a hysterectomy, endometrial ablation or on the Mirena coil, as the ovaries continue to function and the hormonal cycle continues. They can also occur in response to the combined contraceptive pill or cyclical hormone replacement therapy containing progesterone, and this is described as progesterone-induced premenstrual disorder.
When features are severe and have a significant effect on quality of life, this is called premenstrual dysphoric disorder.
How is PMS diagnosed and managed?
Diagnosis is made based on a symptom diary spanning two menstrual cycles. The symptom diary should demonstrate cyclical symptoms that occur just before, and resolve after, the onset of menstruation. A definitive diagnosis may be made, under the care of a specialist, by administering a GnRH analogues to halt the menstrual cycle and temporarily induce menopause, to see if the symptoms resolve.
The following management options can be initiated in primary care:
General healthy lifestyle changes, such as improving diet, exercise, alcohol, smoking, stress and sleep
Combined contraceptive pill (COCP)
SSRI antidepressants
Cognitive behavioural therapy (CBT)
RCOG recommends COCPs containing drospirenone first line (i.e. Yasmin). Drospironone as some antimineralocortioid effects, similar to spironolactone. Continuous use of the pill, as opposed to cyclical use, may be more effective.
Severe cases should be managed by a multidisciplinary team, involving GPs, gynaecologists, psychologists and dieticians.
Continuous transdermal oestrogen (patches) can be used to improve symptoms. Progestogens are required for endometrial protection against endometrial hyperplasia when using oestrogen. This can be in the form of low dose cyclical progestogens (e.g. norethisterone) to trigger a withdrawal bleed, or the Mirena coil.
GnRH analogues can be used to induce a menopausal state. They are very effective at controlling symptoms; however, they are reserved for severe cases due to the adverse effects (e.g. osteoporosis). Hormone replacement therapy can be used to add back the hormones to mitigate these effects.
Hysterectomy and bilateral oophorectomy can be used to induce menopause where symptoms are severe and medical management has failed. Hormone replacement therapy will be required, particularly in women under 45 years.
Danazole and tamoxifen are options for cyclical breast pain, initiated and monitored by a breast specialist.
Spironolactone may be used to treat the physical symptoms of PMS, such as breast swelling, water retention and bloating.
Types of Fibroids
Intramural: within the myometrium (the muscle of the uterus). As they grow, they change the shape and distort the uterus.
Subserosal means (just below the outer layer of the uterus) These fibroids grow outwards and can become very large, filling the abdominal cavity.
Submucosal (just below endometirum)
Pedunculated (on a stalk)
How might fibroids present?
Fibroids are often asymptomatic. They can present in several ways:
Heavy menstrual bleeding (menorrhagia) is the most frequent presenting symptom
Prolonged menstruation, lasting more than 7 days
Abdominal pain, worse during menstruation
Bloating or feeling full in the abdomen
Urinary or bowel symptoms due to pelvic pressure or fullness
Deep dyspareunia (pain during intercourse)
Reduced fertility
Abdominal and bimanual examination may reveal a palpable pelvic mass or an enlarged firm non-tender uterus.
How can fibroids be investigated?
Hysteroscopy is the initial investigation for submucosal fibroids presenting with heavy menstrual bleeding.
Pelvic ultrasound is the investigation of choice for larger fibroids.
MRI scanning may be considered before surgical options, where more information is needed about the size, shape and blood supply of the fibroids.
How are fibroids over 3cm managed?
For fibroids less than 3 cm, the medical management is the same as with heavy menstrual bleeding:
Mirena coil (1st line) – fibroids must be less than 3cm with no distortion of the uterus
Symptomatic management with NSAIDs and tranexamic acid
Combined oral contraceptive
Cyclical oral progestogens
Surgical options for managing smaller fibroids with heavy menstrual bleeding are:
Endometrial ablation
Resection of submucosal fibroids during hysteroscopy
Hysterectomy
Over what side fibroid does a woman need referral to gynecology for investigation and management?
3 cm
How are fibroids over 3cm managed?
For fibroids more than 3 cm, women need referral to gynaecology for investigation and management. Medical management options are:
Symptomatic management with NSAIDs and tranexamic acid (antifibrinolytics)
Mirena coil – depending on the size and shape of the fibroids and uterus
Combined oral contraceptive
Cyclical oral progestogens
Surgical options for larger fibroids are:
Uterine artery embolisation (may preserve fertility)
Myomectomy (usually preserves fertility)
Hysterectomy
Radio frequency ablation to induce necrosis of the fibroid
GnRH agonists, such as goserelin (Zoladex) or leuprorelin (Prostap), may be used to reduce the size of fibroids before surgery. They work by inducing a menopause-like state and reducing the amount of oestrogen maintaining the fibroid. Usually, GnRH agonists are only used short term, for example, to shrink a fibroid before myomectomy.
What is uterine artery embolisation?
Uterine artery embolisation is a surgical option for larger fibroids, performed by interventional radiologists.
The radiologist inserts a catheter into an artery, usually the femoral artery. This catheter is passed through to the uterine artery under X-ray guidance. Once in the correct place, particles are injected that cause a blockage in the arterial supply to the fibroid.
This starves the fibroid of oxygen and causes it to shrink.
Surgical management of fibroids
Myomectomy involves surgically removing the fibroid via laparoscopic (keyhole) surgery or laparotomy (open surgery). Myomectomy is the only treatment known to potentially improve fertility in patients with fibroids.
Endometrial ablation can be used to destroy the endometrium. Second generation, non-hysteroscopic techniques are used, such as balloon thermal ablation. This involves inserting a specially designed balloon into the endometrial cavity and filling it with high-temperature fluid that burns the endometrial lining of the uterus.
Hysterectomy involves removing the uterus and fibroids. Hysterectomy may be by laparoscopy (keyhole surgery), laparotomy or vaginal approach. The ovaries may be removed or left depending on patient preference, risks and benefits.
What treatment can improve fertility in patients with fibroids?
Myomectomy
What are the potential complications of fibroids?
Heavy menstrual bleeding, often with iron deficiency anaemia
Reduced fertility
Pregnancy complications, such as miscarriages, premature labour and obstructive delivery
Constipation
Urinary outflow obstruction and urinary tract infections
Red degeneration of the fibroid
Torsion of the fibroid, usually affecting pedunculated fibroids
Malignant change to a leiomyosarcoma is very rare (<1%)
What is red degeneration of the fibroid?
Ischaemia, infarction and necrosis of the fibroid due to disrupted blood supply.
Which fibroids are more likely to undergo red degeneration?
Red degeneration is more likely to occur in larger fibroids (above 5 cm) during the second and third trimester of pregnancy.
Red degeneration may occur as the fibroid rapidly enlarges during pregnancy, outgrowing its blood supply and becoming ischaemic.
It may also occur due to kinking in the blood vessels as the uterus changes shape and expands during pregnancy.
How does red degeneration of a fibroid present?
Red degeneration presents with severe abdominal pain, low-grade fever, tachycardia and often vomiting.
Management is supportive, with rest, fluids and analgesia.
What is the likely diagnosis for a pregnant woman with a history of fibroids presenting with severe abdominal pain and a low-grade fever
Red degeneration of a fibroid
What is endometriosis?
Endometriosis is a condition where there is ectopic endometrial tissue outside the uterus.
A lump of endometrial tissue outside the uterus is described what?
as an endometrioma.
Endometriomas in the ovaries are often called what?
“chocolate cysts”.
What term refers to endometrial tissue within the myometrium (muscle layer) of the uterus.
Adenomyosis refers to endometrial tissue within the myometrium (muscle layer) of the uterus.
Aetiology of endometriosis?
The exact cause of endometriosis is not clear, but there are several theories.
No specific genes have been found to cause endometriosis; however, there does seem to be a genetic component to developing the condition.
One notable theory for the cause of ectopic endometrial tissue is that during menstruation, the endometrial lining flows backwards, through the fallopian tubes and out into the pelvis and peritoneum.
This is called retrograde menstruation.
The endometrial tissue then seeds itself around the pelvis and peritoneal cavity.
Other possible methods for endometrial tissue exiting the uterus have been proposed:
- Embryonic cells destined to become endometrial tissue may remain in areas outside the uterus during the development of the fetus, and later develop into ectopic endometrial tissue.
- There may be spread of endometrial cells through the lymphatic system, in a similar way to the spread of cancer.
- Cells outside the uterus somehow change, in a process called metaplasia, from typical cells of that organ into endometrial cells.
Pathophysiology of symptoms in endometriosis?
CYCLICAL PAIN - DULL, HEAVY BURNING PAIN:
Endometrial tissue outside the uterus responds to hormones in the same way as endometrial tissue in the uterus. It bleeds during menstruation as it sheds (the same way it does in the uterus) causing irritation and inflammation of the surrounding tissues.
BLOOD IN URINE AND STOOLS
Endometrium deposits in the bowel or bladder
CHRONIC NON-CYCLICAL PAIN - SHARP, STABBING OR PULLING PAIN ASSOCIATED WITH NAEUSEA:
Adhesions form from localised bleeding and inflammation. Scar tissue binds organs together (e.g. ovaries to peritoneum, uterus to bowel)
REDUCED FERTILITY:
Unclear - may be due to adhesions around the ovaries and fallopian tubes blocking the release of eggs or kinking the fallopian tubes obstructing the route to the uterus. Endometriomas in the ovaries may also damage eggs or prevent effective ovulation.
How might endometriosis present?
Asymptomatic
Cyclical: abdominal or pelvic pain, urinary symptoms and bowel symptoms
Deep dyspareunia (pain on deep sexual intercourse)
Dysmenorrhea (painful periods)
Infertility
Cyclical bleeding from other sites such as haematuria
O/E: Endometrial tissue visable in the bagina and on speculum examination, particularly in the posterior fornix, a fixed cervix on bimanual examination, tenderness in the vagina, cervic and adnexa
Endometriosis O/E?
Endometrial tissue visible in the vagina on speculum examination, particularly in the posterior fornix
A fixed cervix on bimanual examination
Tenderness in the vagina, cervix and adnexa
How is endometriosis diagnosis?
Pelvic ultrasound may reveal large endometriomas and chocolate cysts. Ultrasound scans are often unremarkable in patients with endometriosis. Patients with suspected endometriosis need referral to a gynaecologist for laparoscopy.
Laparoscopic surgery is the gold standard way to diagnose abdominal and pelvic endometriosis. A definitive diagnosis can be established with a biopsy of the lesions during laparoscopy. Laparoscopy has the added benefit of allowing the surgeon to remove deposits of endometriosis and potentially improve symptoms.
How is endometreosis staged?
American Society of Reproductive Medicine (ASRM)
Stage 1: Small suoerficial lesions
Stage 2 Mild but deeper lesions than stage 1
Stage 3: Deeper lesion with lesions on the ovaries and mild adhesions
Stage 4: Deep and large lesions affecting the ovaries with extensive adhesions
Existing guidlines fo endometriosis management
RCOG Green-top guideline 41 on chronic pelvic pain (2012), the ESHRE guidelines on endometriosis (2013) and the NICE clinical knowledge summaries (2020).
What does initial management of endometriosis involve?
Establishing a diagnosis
Proving a clear explanation
Listening to the patient establishing ICE and building a partnership
Analgesia as required for pain (NSAIDs and paracetomol first line)
When can hormonal management options for endometresosis be tried and what are they?
Hormonal management options can be tried before establishing a definitive diagnosis with laparoscopy:
Combined oral contractive pill, which can be used back to back without a pill-free period if helpful
Progesterone only pill
Medroxyprogesterone acetate injection (e.g. Depo-Provera)
Nexplanon implant
Mirena coil
GnRH agonists
What treatment of endometriosis may improve fertility?
Laparoscopic surgery to excise or ablate the endometrial tissue and remove adhesions (adhesiolysis)
The aim is to remove as much of the endometriosis as possible, treat adhesions and return the anatomy to normal. This improves fertility in some but not all women with endometriosis.
Surgical management of endometriosis
Laparoscopic surgery to excise or ablate the endometrial tissue and remove adhesions (adhesiolysis)
Hysterectomy
Laparoscopic treatment may improve fertility. Hormonal therapies may improve symptoms but not fertility.
What therapy can treat cyclical pain in endometriosis?
Cyclical pain can be treated with hormonal medications that stop ovulation and reduce endometrial thickening. This can be achieved using the combined oral contraceptive pill, oral progesterone-only pill, the progestin depot injection, the progestin implant (Nexplanon) and the Mirena coil.
The cyclical pain tends to improve after the menopause when the female sex hormones are reduced. Therefore, another treatment option for endometriosis is to induce a menopause-like state using GnRH agonists. Examples of GnRH agonists are goserelin (Zoladex) or leuprorelin (Prostap). They shut down the ovaries temporarily and can be useful in treating pain in many women. However, inducing the menopause has several side effects, such as hot flushes, night sweats and a risk of osteoporosis.
What is the final surgical option to manage endometriosis?
Hysterectomy and bilateral salpingo-opherectomy is the final surgical option. During the procedure, the surgeon will attempt to remove as much of the endometriosis as possible. Importantly, this is still not guaranteed to resolve symptoms. Removing the ovaries induces menopause, and this stops ectopic endometrial tissue responding to the menstrual cycle
Adenomyosis
Adenomyosis refers to endometrial tissue inside the myometrium (muscle layer of the uterus).
It is more common in later reproductive years and those that have had several pregnancies (multiparous). It occurs in around 10% of women overall.
It may occur alone, or alongside endometriosis or fibroids. The cause is not fully understood, and multiple factors are involved, including sex hormones, trauma and inflammation. The condition is hormone-dependent, and symptoms tend to resolve after menopause, similarly to endometriosis and fibroids.
How does pregnancy hx relate to risk of adenomyosis?
Increased risk in multiparity
Cyclical vs non cyclical pain characteristics in endometriosis
NON CYCLICAL = sharp, stabbing or pulling associated with nausea?
Adhesions lead to a chronic, non-cyclical pain that can be sharp, stabbing or pulling and associated with nausea.
CYCLICAL = dull, heavy, burning pain
The cells of the endometrial tissue outside the uterus respond to hormones in the same way as endometrial tissue in the uterus during menstruation and shed as the endometrial tissue in the uterus sheds its lining and bleeds. This causes irritation and inflammation of the tissues around the sites of endometriosis. This results in the cyclical, dull, heavy or burning pain that occurs during menstruation in patients with endometriosis.
Presentation of adenomyosis
Adenomyosis typically presents with:
Painful periods (dysmenorrhoea)
Heavy periods (menorrhagia)
Pain during intercourse (dyspareunia)
It may also present with infertility or pregnancy-related complications. Around a third of patients are asymptomatic.
Examination can demonstrate an enlarged and tender uterus. It will feel more soft than a uterus containing fibroids.
How is adenomyosis diagnosed?
Transvaginal ultrasound of the pelvis is the first-line investigation for suspected adenomyosis.
MRI and transabdominal ultrasound are alternative investigations where transvaginal ultrasound is not suitable.
The gold standard is to perform a histological examination of the uterus after a hysterectomy. However, this is not usually a suitable way of establishing the diagnosis for obvious reasons.
How is adenomyosis managed?
Management of adenomyosis will depend on symptoms, age and plans for pregnancy. NICE recommend the same treatment for adenomyosis as for heavy menstrual bleeding.
When the woman does not want contraception; treatment can be used during menstruation for symptomatic relief, with:
Tranexamic acid when there is no associated pain (antifibrinolytic – reduces bleeding)
Mefenamic acid when there is associated pain (NSAID – reduces bleeding and pain)
Management when contraception is wanted or acceptable:
Mirena coil (first line)
Combined oral contraceptive pill
Cyclical oral progestogens
Progesterone only medications such as the pill, implant or depot injection may also be helpful.
Other options are that may be considered by a specialist include:
GnRH analogues to induce a menopause-like state
Endometrial ablation
Uterine artery embolisation
Hysterectomy
Adenomyosis - complications/associations
Infertility
Miscarriage
Preterm birth
Small for gestational age
Preterm premature rupture of membranes
Malpresentation
Need for caesarean section
Postpartum haemorrhage
What is menopause
Retrospective diagnosis of the end of mensturation
What is postmenopause
Postmenopause describes the period from 12 months after the final menstrual period onwards.
What is perimenopause
Perimenopause refers to the time around the menopause, where the woman may be experiencing vasomotor symptoms and irregular periods. Perimenopause includes the time leading up to the last menstrual period, and the 12 months afterwards. This is typically in women older than 45 years.
Before what age is menopause considered premature?
Premature menopause is menopause before the age of 40 years. It is the result of premature ovarian insufficiency.
What causes menopause?
Menopause is caused by a lack of ovarian follicular function, resulting in changes in the sex hormones associated with the menstrual cycle:
Oestrogen and progesterone levels are low
LH and FSH levels are high, in response to an absence of negative feedback from oestrogen
What is the physiology of menopause?
Decline in development of ovarian follicles
Due to this decrease development there is reduced production of oestrogen by the follicles
The decreased production of oestrogen results in decreased negative feedback on the pituitary gland, therefore more LH and FSH are produced.
As the level of oestrogen falls in the perimenopausal period, there is an absence of negative feedback on the pituitary gland, and increasing levels of LH and FSH.
The failing follicular development means ovulation does not occur (anovulation), resulting in irregular menstrual cycles.
Without oestrogen, the endometrium does not develop, leading to a lack of menstruation (amenorrhoea).
Lower levels of oestrogen also cause the perimenopausal symptoms.
A lack of oestrogen in the perimenopausal period leads to what symptoms?
Hot flushes
Emotional lability or low mood
Premenstrual syndrome
Irregular periods
Joint pains
Heavier or lighter periods
Vaginal dryness and atrophy
Reduced libido
What are post-menopausal women at increased risk of?
A lack of oestrogen increases the risk of certain conditions:
Cardiovascular disease and stroke
Osteoporosis
Pelvic organ prolapse
Urinary incontinence
In which patients is perimenopause a clinical diagnosis?
A diagnosis of perimenopause and menopause can be made in women over 45 years with typical symptoms, without performing any investigations.
NICE guidelines (2015) recommend considering an FSH blood test to help with the diagnosis of menopause in which patients?
Women under 40 years with suspected premature menopause
Women aged 40 – 45 years with menopausal symptoms or a change in the menstrual cycle
Fertility gradually declines after 40 years of age. However, women should still consider themselves fertile. Pregnancy after 40 is associated with increased risks and complications. Post menopausal women need to use effective contraception for how long after their last menstural period?
Two years after the last menstrual period in women under 50
One year after the last menstrual period in women over 50
Why is it difficult to diagnose women on hormonal contraceptives with menopause?
Hormonal contraceptives do not affect the menopause, when it occurs or how long it lasts, although they may suppress and mask the symptoms. This can make diagnosing menopause in women on hormonal contraception more difficult.
What are some good contraceptive options (UKMEC 1) for women approaching the menopause?
Barrier methods
Mirena or copper coil
Progesterone only pill
Progesterone implant
Progesterone depot injection (under 45 years)
Sterilisation
At what age does the COCP become UKMEC 2 (the advantages generally outweigh the risks) ?
after 40
Up to what age can the COCP be if there are no other contraindications?
50 YEARS
In women over 40 taking the COCP pills containing what should be considered and why?
Consider combined oral contraceptive pills containing norethisterone or levonorgestrel in women over 40, due to the relatively lower risk of venous thromboembolism compared with other options.
Why is the progesterone depo injection unsuitable in women over 40?
Two key side effects of the progesterone depot injection (e.g. Depo-Provera): weight gain and reduced bone mineral density (osteoporosis).
These side effects are unique to the depot and do not occur with other forms of contraception.
Reduced bone mineral density makes the depot unsuitable for women over 45 years.
Perimenopausal symtpoms management
No treatment
Hormone replacement therapy (HRT)
Tibolone, a synthetic steroid hormone that acts as continuous combined HRT (only after 12 months of amenorrhoea)
Clonidine, which act as agonists of alpha-adrenergic and imidazoline receptors
Cognitive behavioural therapy (CBT)
SSRI antidepressants, such as fluoxetine or citalopram
Testosterone can be used to treat reduced libido (usually as a gel or cream)
Vaginal oestrogen cream or tablets, to help with vaginal dryness and atrophy (can be used alongside systemic HRT)
Vaginal moisturisers, such as Sylk, Replens and YES
After how long will vasomotor perimenopausal symptoms resolve without any treatment?
2-5 years
What is premature ovarian insufficiency and why might it occur?
Premature ovarian insufficiency is defined as menopause before the age of 40 years.
It is the result of a decline in the normal activity of the ovaries at an early age.
It presents with early onset of the typical symptoms of the menopause.
Premature ovarian insufficiency is characterised by hypergonadotropic hypogonadism. Under-activity of the gonads (hypogonadism) means there is a lack of negative feedback on the pituitary gland, resulting in an excess of the gonadotropins (hypergonadotropism).
Hormonal analysis will show:
Raised LH and FSH levels (gonadotropins)
Low oestradiol levels
Causes of premature ovarian insufficency?
Idiopathic (the cause is unknown in more than 50% of cases)
Iatrogenic, due to interventions such as chemotherapy, radiotherapy or surgery (i.e. oophorectomy)
Autoimmune, possibly associated with coeliac disease, adrenal insufficiency, type 1 diabetes or thyroid disease
Genetic, with a positive family history or conditions such as Turner’s syndrome
Infections such as mumps, tuberculosis or cytomegalovirus
What will hormonal analysis show in premature ovarian insufficiency?
Hormonal analysis will show:
Raised LH and FSH levels (gonadotropins)
Low oestradiol levels
How does premature ovarian insufficiency present?
Premature ovarian insufficiency presents with irregular menstrual periods, lack of menstrual periods (secondary amenorrhea) and symptoms of low oestrogen levels, such has hot flushes, night sweats and vaginal dryness.
How is premature ovarian insufficiency diagnosed?
NICE guidelines on menopause (2015) say premature ovarian insufficiency can be diagnosed in women younger than 40 years with typical menopausal symptoms plus elevated FSH.
The FSH level needs to be persistently raised (more than 25 IU/l) on two consecutive samples separated by more than four weeks to make a diagnosis. The results are difficult to interpret in women taking hormonal contraception.
Women with premature ovarian insufficiency are at higher risk of conditions associated with low oesterogen, such as what?
Cardiovascular disease
Stroke
Osteoporosis
Cognitive impairment
Dementia
Parkinsonism
Management of premature ovarian insufficiency?
Management involves hormone replacement therapy (HRT) until at least the age of 51
HRT reduces the cardiovascular, osteoporosis, cognitive and psychological risks associated with premature menopause.
It is worth noting there is still a small risk of pregnancy in women with premature ovarian failure, and contraception is still required.
There are two options for HRT in women with premature ovarian insufficiency:
Traditional hormone replacement therapy
Combined oral contraceptive pill
HRT vs COCP in managing premature ovarian failure symptoms?
Traditional hormone replacement therapy is associated with a lower blood pressure compared with the combined oral contraceptive pill.
The combined pill may be more socially acceptable (less stigma for younger women) and additionally acts as contraception.
HRT associated breast cancer risk when used to manage premature ovarian insufficiency?
Hormone replacement therapy before the age of 50 is not considered to increase the risk of breast cancer compared with the general population, as women would ordinarily produce the same hormones at this age.
There may be an increased risk of venous thromboembolism with HRT in women under 50 years, how can this risk be reduced?
The risk of VTE can be reduced by using transdermal methods (i.e. patches).
What hormones are involved in HRT and what is their purpose?
Exogenous oestrogen is given to alleviate the symptoms associated with the decline in oestrogen levels during menopause and peri-menopause
Progesterone needs to be given (in addition to oestrogen) to women that have a uterus. The primary purpose of adding progesterone is to prevent endometrial hyperplasia and endometrial cancer secondary to “unopposed” oestrogen.
What is the purpose of progesterone in HRT and which women do not need it?
Prevents endometrial hyperplasia and endometrial cancer secondary to unopposed oestrogen
Only required for women who have a uterus
What type of HRT regime should women that still have periods go on?
Women that still have periods should go on cyclical HRT, with cyclical progesterone and regular breakthrough bleeds.
Postmenopausal women with a uterus and more than 12 months without periods should go on what HRT regime?
Postmenopausal women with a uterus and more than 12 months without periods should go on continuous combined HRT.
Non-hormonal management of menopause (HRT alternatives)
Non-hormonal treatments may be tried initially, or used when there are contraindications to HRT. Options include:
Lifestyle changes such as improving the diet, exercise, weight loss, smoking cessation, reducing alcohol, reducing caffeine and reducing stress
Cognitive behavioural therapy (CBT)
Clonidine, which is an agonist of alpha-adrenergic and imidazoline receptors
SSRI antidepressants (e.g. fluoxetine)
Venlafaxine, which is a selective serotonin-norepinephrine reuptake inhibitor (SNRI)
Gabapentin
Clonidine may be used instead of HRT, how does it work and what side effects may occur?
Clonidine act as an agonist of alpha-2 adrenergic receptors and imidazoline receptors in the brain.
It lowers blood pressure and reduces the heart rate, and is also used as an antihypertensive medication.
It can be helpful for vasomotor symptoms and hot flushes, particularly where there are contraindications to using HRT.
Common side effects of clonidine are dry mouth, headaches, dizziness and fatigue.
Sudden withdrawal can result in rapid increases in blood pressure and agitation.
What herbal remedies might patients try to manage menopause and what problems might they cause?
Black cohosh, which may be a cause of liver damage
Dong quai, which may cause bleeding disorders
Red clover, which may have oestrogenic effects that would be concerning with oestrogen sensitive cancers
Evening primrose oil, which has significant drug interactions and is linked with clotting disorders and seizures
Ginseng may be used for mood and sleep benefits
What are the indications for HRT?
Replacing hormones in premature ovarian insufficiency, even without symptoms
Reducing vasomotor symptoms such as hot flushes and night sweats
Improving symptoms such as low mood, decreased libido, poor sleep and joint pain
Reducing risk of osteoporosis in women under 60 years
Benefits of HRT?
In women under 60 years, the benefits of HRT generally outweigh the risks.
The key benefits to inform women of include:
Improved vasomotor and other symptoms of menopause (including mood, urogenital and joint symptoms)
Improved quality of life
Reduced the risk of osteoporosis and fractures
The risks of HRT are more significant in older women and increase with a longer duration of treatment.
The principal risks of HRT are what?
Increased risk of breast cancer (particularly combined HRT – oestrogen-only HRT has a lower risk)
Increased risk of endometrial cancer
Increased risk of venous thromboembolism (2 – 3 times the background risk)
Increased risk of stroke and coronary artery disease with long term use in older women
The evidence is inconclusive about ovarian cancer, and if there is an increase in risk, it is minimal